請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/50907
完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 郭彥彬 | |
dc.contributor.author | Lih-Jia Huang | en |
dc.contributor.author | 黃俐嘉 | zh_TW |
dc.date.accessioned | 2021-06-15T13:05:45Z | - |
dc.date.available | 2017-08-26 | |
dc.date.copyright | 2016-08-26 | |
dc.date.issued | 2016 | |
dc.date.submitted | 2016-07-05 | |
dc.identifier.citation | Alexander DC, Martin JC, King PJ, Powell JR, Caves J, Cohen ME. 1996. Interleukin-1 beta, prostaglandin E2, and immunoglobulin G subclasses in gingival crevicular fluid in patients undergoing periodontal therapy. Journal of periodontology 67: 755-62
Armitage GC. 1999. Development of a classification system for periodontal diseases and conditions. Annals of periodontology / the American Academy of Periodontology 4: 1-6 Axelsson P, Lindhe J. 1981. Effect of controlled oral hygiene procedures on caries and periodontal disease in adults. Results after 6 years. Journal of clinical periodontology 8: 239-48 Baeuerle PA, Baichwal VR. 1997. NF-kappa B as a frequent target for immunosuppressive and anti-inflammatory molecules. Advances in immunology 65: 111-37 Burger D, Dayer JM, Palmer G, Gabay C. 2006. Is IL-1 a good therapeutic target in the treatment of arthritis? Best practice & research. Clinical rheumatology 20: 879-96 Chabaud M, Page G, Miossec P. 2001. Enhancing Effect of IL-1, IL-17, and TNF- on Macrophage Inflammatory Protein-3 Production in Rheumatoid Arthritis: Regulation by Soluble Receptors and Th2 Cytokines. The Journal of Immunology 167: 6015-20 Claffey N, Polyzois I, Ziaka P. 2004. An overview of nonsurgical and surgical therapy. Periodontology 2000 36: 35-44 Correa MG, Pires PR, Ribeiro FV, Pimentel SZ, Casarin RC, et al. 2016. Systemic treatment with resveratrol and/or curcumin reduces the progression of experimental periodontitis in rats. Journal of periodontal research Cortellini P, Pini Prato G, Tonetti MS. 1993. Periodontal regeneration of human infrabony defects. I. Clinical measures. Journal of periodontology 64: 254-60 Di Benedetto A, Gigante I, Colucci S, Grano M. 2013. Periodontal disease: linking the primary inflammation to bone loss. Clinical & developmental immunology 2013: 5037-54 Dinarello CA, Goldin NP, Wolff SM. 1974. Demonstration and characterization of two distinct human leukocytic pyrogens. The Journal of experimental medicine 139: 1369-81 Garcia RI, Henshaw MM, Krall EA. 2001. Relationship between periodontal disease and systemic health. Periodontology 2000 25: 21-36 Gowen M, Wood DD, Ihrie EJ, McGuire MK, Russell RG. 1983. An interleukin 1 like factor stimulates bone resorption in vitro. Nature 306: 378-80 Guarnieri C, Zucchelli G, Bernardi F, Scheda M, Valentini AF, Calandriello M. 1991. Enhanced superoxide production with no change of the antioxidant activity in gingival fluid of patients with chronic adult periodontitis. Free radical research communications 15: 11-6 Hosokawa Y, Hosokawa I, Ozaki K, Nakae H, Matsuo T. 2005. Increase of CCL20 expression by human gingival fibroblasts upon stimulation with cytokines and bacterial endotoxin. Clinical and experimental immunology 142: 285-91 Hosokawa Y, Hosokawa I, Shindo S, Ozaki K, Matsuo T. 2014. IL-22 enhances CCL20 production in IL-1beta-stimulated human gingival fibroblasts. Inflammation 37: 2062-6 Hosokawa Y, Nakanishi T, Yamaguchi D, Takahashi K, Yumoto H, et al. 2002. Macrophage inflammatory protein 3alpha-CC chemokine receptor 6 interactions play an important role in CD4+ T-cell accumulation in periodontal diseased tissue. Clinical and experimental immunology 128: 548-54 Lee AY, Phan TK, Hulett MD, Korner H. 2015. The relationship between CCR6 and its binding partners: does the CCR6-CCL20 axis have to be extended? Cytokine 72: 97-101 Lin JK, Pan MH, Lin-Shiau SY. 2000. Recent studies on the biofunctions and biotransformations of curcumin. BioFactors (Oxford, England) 13: 153-8 Loe H. 1993. Periodontal diseases: a brief historical perspective. Periodontology 2000 2: 7-12 Mendes AF, Caramona MM, Carvalho AP, Lopes MC. 2003. Differential roles of hydrogen peroxide and superoxide in mediating IL-1-induced NF-kappa B activation and iNOS expression in bovine articular chondrocytes. Journal of cellular biochemistry 88: 783-93 Moseley R, Waddington RJ, Embery G, Rees SG. 1998. The modification of alveolar bone proteoglycans by reactive oxygen species in vitro. Connective tissue research 37: 13-28 Preiss DS, Meyle J. 1994. Interleukin-1 beta concentration of gingival crevicular fluid. Journal of periodontology 65: 423-8 Pulikkotil SJ, Nath S. 2015. Effects of curcumin on crevicular levels of IL-1beta and CCL28 in experimental gingivitis. Australian dental journal 60: 317-27 Socransky SS, Haffajee AD. 1991. Microbial mechanisms in the pathogenesis of destructive periodontal diseases: a critical assessment. Journal of periodontal research 26: 195-212 Stashenko P, Jandinski JJ, Fujiyoshi P, Rynar J, Socransky SS. 1991. Tissue levels of bone resorptive cytokines in periodontal disease. Journal of periodontology 62: 504-9 Tanida S, Yoshitomi H, Nishitani K, Ishikawa M, Kitaori T, et al. 2009. CCL20 produced in the cytokine network of rheumatoid arthritis recruits CCR6+ mononuclear cells and enhances the production of IL-6. Cytokine 47: 112-8 Thornberry NA, Bull HG, Calaycay JR, Chapman KT, Howard AD, et al. 1992. A novel heterodimeric cysteine protease is required for interleukin-1 beta processing in monocytes. Nature 356: 768-74 Tuter G, Kurtis B, Serdar M. 2001. Interleukin-1beta and thiobarbituric acid reactive substance (TBARS) levels after phase I periodontal therapy in patients with chronic periodontitis. Journal of periodontology 72: 883-8 Valko M, Leibfritz D, Moncol J, Cronin MT, Mazur M, Telser J. 2007. Free radicals and antioxidants in normal physiological functions and human disease. The international journal of biochemistry & cell biology 39: 44-84 Waddington RJ, Moseley R, Embery G. 2000. Reactive oxygen species: a potential role in the pathogenesis of periodontal diseases. Oral diseases 6: 138-51 Wilson KP, Black JA, Thomson JA, Kim EE, Griffith JP, et al. 1994. Structure and mechanism of interleukin-1 beta converting enzyme. Nature 370: 270-5 | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/50907 | - |
dc.description.abstract | Periodontal diseases have a high prevalence in Taiwan. The primary cause of periodontitis is poor or ineffective oral hygiene, which leads to the accumulation of bacterial matrix, called dental plaque. Subgingival micro-organisms would deposit endotoxin and cause further inflammation in the gum tissues and progressive bone loss. During the inflammation process, a lot of cytokines will increases in expression. One of them is Interleukin-1β (IL-1β). IL-1βhas the ability to induce Chemokine (C-C motif) ligand 20 (CCL20), and CCL20 can attract T helper cell to the inflamed gingival tissue, causing IL-17 to increase. Il-17 can promote osteoclast activity and subsequently escalate bone resorption. The overall mechanism involved in the induction of CCL20 by IL-1β is still unknown and it is the aim of our study to further investigate this signaling pathway.
Previous studies had shown that IL-1βinduce CCL20 in Human gingival fibroblast (HGF) via a NF-κB dependent pathway. We discovered the NOX4 inhibitor, Plumbagin and ROS inhibitor, NAC can inhibit the above mentioned pathway. And IL-1β can induce NOX4 and ROS in HGF as well. This proved that the signaling pathway of CCL20 induction by IL-1βis NOX4 dependent. Furthermore, we also discovered that Curcumin has the ability to inhibit IL-1β from inducing NOX4 and CCL20 in HGF. This finding may be useful in developing future adjunctive therapy in treating periodontal disease. | en |
dc.description.provenance | Made available in DSpace on 2021-06-15T13:05:45Z (GMT). No. of bitstreams: 1 ntu-105-R02422005-1.pdf: 991569 bytes, checksum: 3a67ddc64f3dd7f53be7824910fbda8f (MD5) Previous issue date: 2016 | en |
dc.description.tableofcontents | 目錄
口試委員會審定書………………………………………………………………….I 誌謝 …………………………………………………………………………………II 中文摘要 ……………………………………………………………………………III Abstract………………………………………………………………………………IV 第一章 導論 第一節 糖尿病 1-1 牙周病的簡介……………………………………………………………1 1-2 牙周病的流行病學………………………………………………………1 1-3 牙周病的致病機轉………………………………………………………2 1-4 牙周病的治療……………………………………………………………3 第二節 介白素-1β (Interleukin-1β) 2-1 介白素-1β…………...……………………………………………………4 2-2 介白素-1β與牙周病……………….……………………………………4 第三節CC趨化因子20 (CCL20) 3-1 CC趨化因子20的簡介…………………………………………………5 3-2 CCL20與牙周病的關係子………………………………………………5 3-3 CCL20與IL-1β的關係………………………………………………….6 第四節 過氧化物 4-1過氧化物的簡介………………………………………………………….6 4-2 ROS與牙周病的關.………………………………………………………7 第五節 薑黃素 (Curcumin)……………………………………………………...7 第二章 實驗目的 …………………………………………………………………8 第三章 實驗材料與方法 第一節 牙齦檢體的收集 ………………………………………………………9 第二節 人類牙齦纖維母細胞之初代培養 ……………………………………9 第三節 人類頰黏膜纖維母細胞之繼代培養…………………………………9 第四節 藥物處理………………………………………………………………10 第五節 西方墨點法 (Western Blot) ………………………………………11 第六節 Enzyme-linked Immunosorbent Assay(ELISA)……………………12 第七節 流式細胞儀檢測過氧化物含量………………………………………13 第八節 si-RNA 轉染 (Transfection)………………………………………13 第九節 統計方法………………………………………………………………13 第四章 結果 IL-1β誘導CCL20之生成 ……………………………………………………14 IL-1β誘導CCL20之時間點 …………………………………………………14 IL-1β經由NF-κB誘導HGF內的CCL20表現量……………………………14 Curcumin可抑制HGF內IL-1β誘導的CCL20表現量………………………15 IL-1β經由NOX4誘導HGF內的CCL20表現量………………………………15 Curcumin可抑制HGF內IL-1β誘導的ROS與NOX4之表現量 ……………16 第五章 討論 ………………………………………………………………………17 第六章 總結及未來之展望 ………………………………………………………18 第七章 圖與表 ……………………………………………………………………19 第八章 參考文獻 …………………………………………………………………30 | |
dc.language.iso | zh-TW | |
dc.title | IL-1β經由NOX4誘導人類牙齦纖維母細胞CC趨化因子20生成 | zh_TW |
dc.title | NADPH Oxidase 4 Mediates IL-1β induced CCL20 in Human Gingival Fibroblasts | en |
dc.type | Thesis | |
dc.date.schoolyear | 104-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 張瑞青,周涵怡 | |
dc.subject.keyword | 牙周病,人類牙齦纖維母細胞,IL-1β,CCL20,過氧化物,NOX4,薑黃素, | zh_TW |
dc.subject.keyword | Periodontitis,Human gingival fibroblast,IL-1β,CCL20,ROS,NOX4,Curcumin, | en |
dc.relation.page | 33 | |
dc.identifier.doi | 10.6342/NTU201600684 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2016-07-05 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 臨床牙醫學研究所 | zh_TW |
顯示於系所單位: | 臨床牙醫學研究所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
---|---|---|---|
ntu-105-1.pdf 目前未授權公開取用 | 968.33 kB | Adobe PDF |
系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。